Kuropka Benno, Witte Amelie, Sticht Jana, Waldt Natalie, Majkut Paul, Hackenberger Christian P R, Schraven Burkhart, Krause Eberhard, Kliche Stefanie, Freund Christian
From the ‡Freie Universität Berlin, Institut für Chemie und Biochemie, Protein Biochemistry group, Thielallee 63, 14195 Berlin, Germany; §Leibniz-Institut für Molekulare Pharmakologie, Robert-Rössle-Strasse 10, 13125 Berlin, Germany;
¶Otto-von-Guericke-University, Institute of Molecular and Clinical Immunology, Leipziger Strasse 44, 39120 Magdeburg, Germany;
Mol Cell Proteomics. 2015 Nov;14(11):2961-72. doi: 10.1074/mcp.M115.048249. Epub 2015 Aug 5.
Stimulation of T cells leads to distinct changes of their adhesive and migratory properties. Signal propagation from activated receptors to integrins depends on scaffolding proteins such as the adhesion and degranulation promoting adaptor protein (ADAP)(1). Here we have comprehensively investigated the phosphotyrosine interactome of ADAP in T cells and define known and novel interaction partners of functional relevance. While most phosphosites reside in unstructured regions of the protein, thereby defining classical SH2 domain interaction sites for master regulators of T cell signaling such as SLP76, Fyn-kinase, and NCK, other binding events depend on structural context. Interaction proteomics using different ADAP constructs comprising most of the known phosphotyrosine motifs as well as the structured domains confirm that a distinct set of proteins is attracted by pY571 of ADAP, including the ζ-chain-associated protein kinase of 70 kDa (ZAP70). The interaction of ADAP and ZAP70 is inducible upon stimulation either of the T cell receptor (TCR) or by chemokine. NMR spectroscopy reveals that the N-terminal SH2 domains within a ZAP70-tandem-SH2 construct is the major site of interaction with phosphorylated ADAP-hSH3(N) and microscale thermophoresis (MST) indicates an intermediate binding affinity (Kd = 2.3 μm). Interestingly, although T cell receptor dependent events such as T cell/antigen presenting cell (APC) conjugate formation and adhesion are not affected by mutation of Y571, migration of T cells along a chemokine gradient is compromised. Thus, although most phospho-sites in ADAP are linked to T cell receptor related functions we have identified a unique phosphotyrosine that is solely required for chemokine induced T cell behavior.
T细胞的刺激会导致其黏附性和迁移特性发生明显变化。从活化受体到整合素的信号传导依赖于支架蛋白,如黏附与脱颗粒促进衔接蛋白(ADAP)(1)。在此,我们全面研究了T细胞中ADAP的磷酸酪氨酸相互作用组,并确定了功能相关的已知和新型相互作用伙伴。虽然大多数磷酸化位点位于蛋白质的无结构区域,从而为T细胞信号传导的主要调节因子(如SLP76、Fyn激酶和NCK)定义了经典的SH2结构域相互作用位点,但其他结合事件则取决于结构背景。使用包含大多数已知磷酸酪氨酸基序以及结构化结构域的不同ADAP构建体进行的相互作用蛋白质组学证实,ADAP的pY571吸引了一组独特的蛋白质,包括70 kDa的ζ链相关蛋白激酶(ZAP70)。ADAP与ZAP70的相互作用在T细胞受体(TCR)刺激或趋化因子刺激后均可诱导。核磁共振光谱显示,ZAP70串联SH2构建体中的N端SH2结构域是与磷酸化ADAP-hSH3(N)相互作用的主要位点,微量热泳动(MST)表明其具有中等结合亲和力(Kd = 2.3 μm)。有趣的是,虽然T细胞受体依赖性事件,如T细胞/抗原呈递细胞(APC)共轭形成和黏附不受Y571突变的影响,但T细胞沿趋化因子梯度的迁移受到损害。因此,尽管ADAP中的大多数磷酸化位点与T细胞受体相关功能有关,但我们已经鉴定出一个独特的磷酸酪氨酸,它是趋化因子诱导的T细胞行为所特需的。